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INFLUENCE OF EXTRACELLULAR pH, SODIUM PROPIONATE AND TRIMETHYLAMINE ON EXCITATION‐CONTRACTION COUPLING IN THE RAT TAIL ARTERY
Author(s) -
Achike Francis I.,
Ballard Heather J.,
Ogle Clive W.
Publication year - 1996
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1996.tb02586.x
Subject(s) - extracellular , contraction (grammar) , intracellular ph , chemistry , intracellular , calcium , medicine , endocrinology , acidosis , alkalosis , sodium , biophysics , extracellular fluid , biochemistry , biology , organic chemistry
SUMMARY 1. The effects of extracellular or intracellular pH changes on agonist‐ or depolarization‐induced contractions of the rat tail artery were investigated. 2. Vessels were perfused initially (25 min) with physiological salt solution (PSS) at a pressure of 30 mmHg. Perfusion was then continued with calcium‐free PSS containing either 3.0 μmol/L noradrenaline (NA) or 100 mmol/L K + , which had been made either acidotic or alkalotic. Contractile responses to graded concentrations of calcium were assessed. 3. A reduction in the intracellular or extracellular pH was induced by the addition of a weak acid (30 mmol/L sodium propionate) or reduction of the concentration of HCO 3 ‐ in the PSS, respectively; an elevation of the intracellular or extracellular pH was produced by the addition of a weak base (10 mmol/L trimethylamine) or by increasing HCO 3 ‐ , respectively. The PSS was bubbled with 5% CO 2 /95% O 2. 4. Lowered intracellular pH did not alter NA‐ or K + ‐stimulated contractions. During lowered extracellular pH, contractile responsiveness and peak response were significantly reduced in K + ‐stimulated arteries, but were not affected in NA‐stimulated arteries. 5. Elevated intracellular pH did not alter NA‐induced contraction, but reduced the sensitivity to K + ‐stimulated contractions. Elevated extracellular pH had little effect on the magnitude of K + ‐induced contractions, but slightly enhanced (although not significantly) NA‐induced contractions. 6. It is concluded that reduced contractile responses to K + during extracellular acidosis are due to the modulation of potential‐operated calcium channels (POC). Alkalotic vasodilatation is mediated by intracellular events and is POC‐modulated, whereas alkalotic vasoconstriction appears to be due to extracellular events and is modulated by receptor‐operated calcium channels (ROC).